Most bacteria isolated from the human oral cavity possess the ability to participate in intergeneric coaggregation (bacteria from different genera bind to each other primarily via a protein on one attaching to a saccharide component on the other). Coaggregation is characterized by a highly specific binding between stable surface components found on two different bacterial types. Intergeneric coaggregation is thought to play an important role in the formation of dental plaque deposits (10, 11). Streptococcus oralis is one of the earliest colonizers of the clean tooth surface and is found in significant numbers in dental plaque (4, 19). The interaction between Streptococcus oralis H1 ATCC55229 and Capnocytophaga ochracea ATCC 33596 was first described by Kolenbrander and Andersen (9). A study (22) demonstrated that L-rhamnose and D-fucose were the most effective inhibitors of this coaggregation while galactosides, i.e. B-methyl galactoside, D-galactose, lactose and o-methyl galactoside were less effective inhibitors.
Thus far, the only bacterial carbohydrate receptor for a bacterial lectin studied in detail is the carbohydrate receptor on Streptococcus oralis 34 that is recognized by the adhesin on Actinomyces viscosus T14V. This interaction is inhibited by .beta.-galactosides and B-N-acetylgalactosaminides. A cell wall coaggregation-inhibiting polysaccharide antigen from Streptococcus oralis 34 has been isolated and characterized (16). This polysaccharide consists of rhamnose, glucose, galactose and N-acetyl galactosamine in a hexasaccharide repeating unit (15). The polysaccharide inhibits coaggregation, contains saccharide components that by themselves are effective inhibitors of the interaction, and is a major cell surface antigen (16).
The available technology in combating dental plaque comprises the use of toothpastes, mouth washes, chewing gum, etc., which all work in a non-specific fashion, primarily by means of detergents and abrasives.